International heart journal最新文献

The clinical manifestations of licorice-induced pseudoaldosteronism include muscle weakness, periodic paralysis, hypokalemia, and hypertension. Excessive licorice consumption can lead to adverse reactions affecting multiple systems, including the endocrine, cardiovascular, nervous, digestive, and immune systems. Although licorice is a frequently used Chinese herbal medicine, life-threatening adverse reactions have been reported among its users. This article presents a case of severe hypokalemia, torsade de pointes, severe hypertension, and exacerbation of manic symptoms resulting from an overdose of compound licorice tablets. This study aimed to enhance the understanding of the causes of hypokalemia and raise awareness on the potentially fatal adverse reactions associated with licorice drugs.

This study aimed to evaluate the clinical value of circ_0008842 in acute myocardial infarction (AMI) and explore the potential mechanisms.

GSE149051 and GSE160717 datasets analyze common differentially expressed circRNAs (coDEcircRNA) in AMI. RT-qPCR analysis of circ_0008842 mRNA levels in patients with AMI. ROC curve assesses the diagnostic value of circ_0008842 in AMI. A cell model of AMI was constructed by hypoxia-reoxygenation (H/R) -induced H9c2. Cell viability and apoptosis were examined by CCK-8 and flow cytometry. Enzyme-linked immunosorbent assay was used to explore myocardial injury markers CK-MB and cTnI secretion. Dual luciferase reporter assays validate circ_0008842 binding to miRNA. PPI network and gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment reveal potential functions and pathways of targets from the miRNA in AMI.

circ_0008842 is recognized as coDEcircRNA in AMI-related databases. circ_0008842 was greatly lower and miR-574-5p was significantly higher in patients with AMI than in healthy individuals. miR-574-5p is a target of circ_0008842. The sensitivity and specificity of circ_0008842 for diagnosing patients with AMI were 87.40% and 83.50%, respectively. Overexpression of circ_0008842 inhibited H/R induced apoptosis, increased cell viability, and decreased CK-MB and cTnI levels, which were partially abrogated by overexpression of miR-574-5p. Calmodulin-like protein 4 (CALML4) was the most connected hub gene in the PPI network of miR-574-5p predicted target genes.

circ_0008842 is a diagnostic biomarker for AMI and participates in myocardial injury in AMI by regulating miR-574-5p. Our study provides new insights into the diagnosis for AMI.

This study aimed to investigate the predictive value of advanced lung cancer inflammation index (ALI) for major adverse cardiovascular events (MACEs) in elderly patients with acute coronary syndrome (ACS).

A total of 586 ACS patients undergoing percutaneous coronary intervention (PCI) over 65 years old between January 2017 and December 2018 were retrospectively collected. The patients were divided into two groups by the optimal cutoff value of ALI. Spearman rank correlation coefficient was used to evaluate the correlation between ALI and the Global Registry of Acute Coronary Events (GRACE). Time-dependent receiver operating characteristic (ROC) curves, Cox survival analysis, and Kaplan Meier curves were used to assess the predictive value of ALI for MACEs.

Spearman's nonparametric test revealed a moderate correlation between ALI and the GRACE (r: −0.417, P < 0.001). Time-dependent ROC curves showed that the area under the curve for ALI was 0.751 (95% CI, 0.699-0.798) in predicting MACEs, higher than Geriatric Nutritional Risk Index (0.531, 95% CI 0.435-0.627) and Prognostic Nutritional Index (0.590, 95% CI 0.505 - 0.676), and for combined diagnostic models (ALI + GRACE) was 0.913, (95% CI 0.875 - 0.942, P < 0.001). Multivariate Cox analysis demonstrated that ALI (HR: 0.974, 95% CI: 0.952-0.996, P = 0.017) was an independent risk factor for MACEs. Kaplan Meier survival analysis showed that the cumulative incidence of MACEs was significantly higher in elderly ACS patients with lower ALI (log-rank test, P < 0.001).

ALI could be a nutrition-inflammation indicator with independent predictive value for long-term MACEs of elderly ACS patients after PCI.

Dextrocardia is a very rare congenital malposition, and most cardiologists are not familiar with the radiographic angiograms of this condition. Here, we first report a case of dextrocardia with a chronic total occlusion (CTO) lesion undergoing retrograde percutaneous coronary intervention (PCI). Significant difficulties in lesion interpretation and device manipulation were encountered with the original angiograms. These challenges were not significantly improved until we adopted the double-inversion technique. The procedure was finally accomplished by using the kissing wire technique with a poor angle of attack. Retrograde CTO PCI for patients with dextrocardia is feasible with adequate techniques.

Pulmonary hypertension (PH) is a complex cardiovascular condition that is characterized by elevated pulmonary arterial pressure, which leads to significant morbidity and mortality. Among the various factors that influence the pathophysiology and progression of PH, iron deficiency has become a critical, yet often overlooked, element. In this review, the prevalence, implications, and therapeutic potential of addressing iron deficiency in patients with PH are elucidated.

Iron deficiency, which is prevalent in a significant proportion of patients with PH, has been associated with worsened clinical outcomes, including diminished exercise capacity, impaired oxygen transport and utilization, and compromised right ventricular function. The pathophysiological linkages between iron deficiency and PH are multifaceted and involve alterations in oxygen sensing, endothelial function, and metabolic disturbances.

In this review, the evidence from recent clinical trials and studies that assess the impact of iron supplementation, both oral and intravenous, on PH outcomes is critically analyzed. Although some studies suggest improvements in exercise capacity and hemodynamic parameters following iron repletion, the responses appear variable and are not universally beneficial. This review highlights the complexities of iron metabolism in PH and the challenges in effectively diagnosing and treating iron deficiency in this patient population.

Furthermore, the potential mechanisms through which iron supplementation might influence pulmonary vascular and right ventricular function, emphasizing the need for personalized treatment approaches are discussed. In this review, the importance of recognizing iron deficiency in the management of patients with PH is highlighted, and further research is warranted to establish comprehensive, evidence-based guidelines for iron supplementation in this unique patient cohort. The ultimate goal of this review is to improve clinical outcomes and quality of life for patients suffering from this debilitating condition.

When stimulated, vascular smooth muscle cells (VSMCs) change from a differentiated to a dedifferentiated phenotype. Dedifferentiated VSMCs have a key activity in cardiovascular diseases such as in-stent restenosis. MicroRNAs (miRNAs) have crucial functions in conversion of differentiated VSMCs to a dedifferentiated phenotype. We investigated the activity of miR-411-5p in the proliferation, migration, and phenotype switch of rat VSMCs.

Based on a microRNA array assay, miR-411-5p expression was found to be significantly increased in cultured VSMCs stimulated by platelet-derived growth factor-BB (PDGF-BB). A CCK-8 assay, transwell assay, and scratch test were performed to measure the effect of miR-411-5p on the proliferation and migration of PDGF-BB-treated VSMCs. MiR-411-5p promoted expression of dedifferentiated phenotype markers such as osteopontin and tropomyosin 4 in PDGF-BB-treated VSMCs. Using mimics and inhibitors, we identified the target of miR-411-5p in PDGF-BB-treated VSMCs and found that calmodulin-regulated spectrin-associated protein-1 (CAMSAP1) was involved in the phenotypic switch mediated by PDGF-BB.

By inhibiting expression of CAMSAP1, miR-411-5p enhanced the proliferation, migration, and phenotype switch of VSMCs.

Blockade of miR-411-5p interaction with CAMSAP1 is a promising approach to treat in-stent restenosis.

This study aimed to clarify (1) the association among the atrial fibrillation (AF) type, sleep-disordered breathing (SDB), heart failure (HF), and left atrial (LA) enlargement, (2) the independent predictors of LA enlargement, and (3) the effects of ablation on those conditions in patients with AF. The study's endpoint was LA enlargement (LA volume index [LAVI] ≥ 78 mL/m²).

Of 423 patients with nonvalvular AF, 236 were enrolled. We evaluated the role of the clinical parameters such as the AF type, SDB severity, and HF in LA enlargement. Among them, 141 patients exhibiting a 3% oxygen desaturation index (ODI) of ≥ 10 events/hour underwent polysomnography to evaluate the SDB severity measured by the apnea-hypopnea index (AHI). The LA enlargement and HF were characterized by the LA diameter/LAVI, an increase in the B-type natriuretic peptide level, and a lower left ventricular ejection fraction.

This study showed that non-paroxysmal AF (NPAF) rather than paroxysmal AF (PAF), the SDB severity, LA enlargement, and HF progression had bidirectional associations and exacerbated each other, which generated a vicious cycle that contributed to the LA enlargement. NPAF (OR = 4.55, P < 0.001), an AHI of ≥ 25.10 events/hour (OR = 1.55, P = 0.003), and a 3% ODI of ≥ 15.43 events/hour (OR = 1.52, P = 0.003) were independent predictors of an acceleration of the LA enlargement. AF ablation improved the HF and LA enlargement.

To break this vicious cycle, AF ablation may be the basis for suppressing the LA enlargement and HF progression subsequently eliminating the substrates for AF and SDB in patients with AF.

Hydrogen sulfide (H₂S) has been identified as a novel gasotransmitter and a substantial antioxidant that can activate various cellular targets to regulate physiological and pathological processes in mammals. However, under physiological conditions, it remains unclear whether it is involved in regulating cardiomyocyte (CM) proliferation during postnatal development in mice. This study mainly aimed to evaluate the role of H₂S in postnatal CM proliferation and its regulating molecular mechanisms. We found that sodium hydrosulfide (NaHS, the most widely used H₂S donor, 50-200 μM) increased neonatal mouse primary CM proliferation in a dose-dependent manner in vitro. Consistently, exogenous administration of H₂S also promoted CM proliferation and increased the total number of CMs at postnatal 7 and 14 days in vivo. Moreover, we observed that the protein expression of SIRT1 was significantly upregulated after NaHS treatment. Inhibition of SIRT1 with EX-527 or si-SIRT1 decreased CM proliferation, while enhancement of the activation of SIRT1 with SRT1720 promoted CM proliferation. Meanwhile, pharmacological and genetic blocking of SIRT1 repressed the effect of NaHS on CM proliferation. Taken together, these results reveal that H₂S plays a promotional role in proliferation of CMs in vivo and in vitro and SIRT1 is required for H₂S-mediated CM proliferation, which indicates that H₂S may be a potential modulator for heart development in postnatal time window.

Late kidney injury (LKI) in patients with acute heart failure (AHF) requiring intensive care is poorly understood.

We analyzed 821 patients with AHF who required intensive care. We defined LKI based on the ratio of the creatinine level 1 year after admission for AHF to the baseline creatinine level. The patients were categorized into 4 groups based on this ratio: no-LKI (< 1.5, n = 509), Class R (risk; ≥ 1.5, n = 214), Class I (injury; ≥ 2.0, n = 78), and Class F (failure; ≥ 3.0, n = 20). Median follow-up after admission for AHF was 385 (346-426) days. Multivariate logistic regression analysis revealed that acute kidney injury (AKI) during hospitalization (Class R, odds ratio [OR]: 1.710, 95% confidence interval [CI]: 1.138-2.571, P = 0.010; Class I, OR: 6.744, 95% CI: 3.739-12.163, P < 0.001; and Class F, OR: 9.259, 95% CI: 4.078-18.400, P < 0.001) was independently associated with LKI. Multivariate Cox regression analysis showed that LKI was an independent predictor of 3-year all-cause death after final follow-up (hazard ratio: 1.545, 95% CI: 1.099-2.172, P = 0.012). The rate of all-cause death was significantly lower in the no-AKI/no-LKI group than in the no-AKI/LKI group (P = 0.048) and in the AKI/no-LKI group than in the AKI/LKI group (P = 0.017).

The incidence of LKI was influenced by the presence of AKI during hospitalization, and was associated with poor outcomes within 3 years of final follow-up. In the absence of LKI, AKI during hospitalization for AHF was not associated with a poor outcome.

Periodontitis is a common chronic infection and is associated with cardiovascular disease. This study evaluated whether basic oral care for periodontal disease could improve endothelial function in patients with acute coronary syndrome (ACS).

This study enrolled 54 patients with acute coronary syndrome admitted to Kagoshima City Hospital and who had undergone percutaneous coronary intervention. Flow-mediated endothelium-dependent dilatation (FMD) was measured before discharge (initial FMD) and at 8 months after percutaneous coronary intervention (follow-up FMD). The following periodontal characteristics were measured: periodontal pocket depth (PPD, mm), plaque control record (%), and bleeding on probing (%). All patients received basic oral care instructions from dentists. The oral health condition was generally poor in the participants and there were 24 patients (44.4%) who had severe PPD. Despite the intervention of basic oral care, the periodontal characteristics did not improve during the study period; initial FMD and follow-up FMD did not significantly differ (4.38 ± 2.74% versus 4.56 ± 2.51%, P = 0.562). However, the follow-up FMD was significantly lower in patients with severe PPD (≥ 6.0 mm, n = 24) than in patients without severe PPD (≤ 5.0 mm, n = 30) (FMD: 3.58 ± 1.91% versus 5.37 ± 2.67%, P = 0.007). FMD tended to be worse in patients with severe PPD than in patients without severe PPD (ΔFMD: -0.55 ± 2.12 versus 0.81 ± 2.77 %, P = 0.055). In conclusion, during the use of basic oral care, endothelial function improved in patients without severe PPD, while it worsened in patients with severe PPD.